Evidence map›Paper›PMID 31312757›Full record

ArticleJACC. Basic to translational science2019

Cathepsin A Mediates Ventricular Remote Remodeling and Atrial Cardiomyopathy in Rats With Ventricular Ischemia/Reperfusion.

Mathias Hohl, Katharina Erb, Lisa Lang, Sven Ruf, Thomas Hübschle, Stefan Dhein, Wolfgang Linz, Adrian D Elliott, Prashanthan Sanders, Olesja Zamyatkin and 4 more

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Histone Deacetylase 6 Controls Atrial Fibrosis and Remodeling in Postinfarction Mice Through the Modulation of Wnt3a/GSK-3β Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 7 institutions in 3 countries.

Mathias HohlKlinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
Katharina ErbKlinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
Lisa LangKlinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
Sven RufSanofi-Aventis Deutschland GmbH, Frankfurt, Germany.
Thomas HübschleSanofi-Aventis Deutschland GmbH, Frankfurt, Germany.
Stefan DheinHerzzentrum Leipzig Abt. Herzchirurgie, Leipzig, Germany.
Wolfgang LinzSanofi-Aventis Deutschland GmbH, Frankfurt, Germany.
Adrian D ElliottCentre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia.
Prashanthan SandersCentre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia.
Olesja ZamyatkinKlinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
Michael BöhmKlinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
Ulrich SchottenDepartment of Physiology, University of Maastricht, Maastricht, the Netherlands.
Thorsten SadowskiSanofi-Aventis Deutschland GmbH, Frankfurt, Germany.
Dominik LinzKlinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
Saarland University · DESanofi (Germany) · DEDeutsches Herzzentrum der Charité · DEMaastricht University · NLRoyal Adelaide Hospital · AUSouth Australian Health and Medical Research Institute · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After myocardial infarction, remote ventricular remodeling and atrial cardiomyopathy progress despite successful revascularization. In a rat model of ventricular ischemia/reperfusion, pharmacological inhibition of the protease activity of cathepsin A initiated at the time point of reperfusion prevented extracellular matrix remodeling in the atrium and the ventricle remote from the infarcted area. This scenario was associated with preservation of more viable ventricular myocardium and the prevention of an arrhythmogenic and functional substrate for atrial fibrillation. Remote ventricular extracellular matrix remodeling and atrial cardiomyopathy may represent a promising target for pharmacological atrial fibrillation upstream therapy following myocardial infarction.

Indexed as

AF, atrial fibrillationatrial cardiomyopathyatrial fibrillationCatA, cathepsin ACx43, connexin 43ECM, extracellular matrixICM, ischemic cardiomyopathyI/R, ischemia/reperfusionischemia/reperfusionLAD, left anterior descending coronary arteryLA, left atrialLV, left ventricularMRI, magnetic resonance imagingmRNA, messenger ribonucleic acidmyocardial infarctionPL, permanent left anterior descending ligationremote remodelingSAR, (S)-3-{[1-(2-Fluoro-phenyl)-5-methoxy-1H-pyrazole-3-carbonyl]-amino}-3-o-tolyl-propionic-acid

Identifiers

PMID31312757
PMCPMC6609908
OpenAlexW2955692977

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.